Figure 3.
Deficiency of FLOT2 in LIC does not alter disease course in MLL–AF9-driven AML. (A) Leukocyte counts × 103/μL, (n.s.; t test; n = 11) in PB of WT mice transplanted with MLL-AF9+ BM from WT (red) or Flot2 KO (blue) mice 34 days after transplantation. (B) Kaplan-Meier-style survival curve of WT recipient mice transplanted with BM from WT (solid line, red) or Flot2 KO (dashed line, blue) mice, transduced with MLL–AF9-expressing retrovirus (n.s.; log-rank test; n = 11-12). (C-D) Percentage of total leukocytes (n. s.; t test; n = 5) (C) and absolute number per femur of GFP+ (MLL-AF9+) WT (black) or Flot2 KO (blue) LKS cells (n.s.; t test; n = 5) (D), which homed to the BM of WT mice 18 hours after transplantation. (E) Quantification of proviral integration sites by LDI PCR on DNA derived from spleens of WT mice which had been transplanted with WT (red) or Flot2 KO (blue) MLL-AF9-transduced BM in the AML model (n.s.; t test; n = 9-10).

Deficiency of FLOT2 in LIC does not alter disease course in MLL–AF9-driven AML. (A) Leukocyte counts × 103/μL, (n.s.; t test; n = 11) in PB of WT mice transplanted with MLL-AF9+ BM from WT (red) or Flot2 KO (blue) mice 34 days after transplantation. (B) Kaplan-Meier-style survival curve of WT recipient mice transplanted with BM from WT (solid line, red) or Flot2 KO (dashed line, blue) mice, transduced with MLL–AF9-expressing retrovirus (n.s.; log-rank test; n = 11-12). (C-D) Percentage of total leukocytes (n. s.; t test; n = 5) (C) and absolute number per femur of GFP+ (MLL-AF9+) WT (black) or Flot2 KO (blue) LKS cells (n.s.; t test; n = 5) (D), which homed to the BM of WT mice 18 hours after transplantation. (E) Quantification of proviral integration sites by LDI PCR on DNA derived from spleens of WT mice which had been transplanted with WT (red) or Flot2 KO (blue) MLL-AF9-transduced BM in the AML model (n.s.; t test; n = 9-10).

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